Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, SP, Brazil.
Exp Physiol. 2023 Mar;108(3):361-370. doi: 10.1113/EP090912. Epub 2023 Jan 30.
What is the central question of this study? Is the cardiovascular phenotype of high blood pressure observed in rats salt loaded with 2% NaCl in drinking solution a blood volume-dependent hypertension? What is the main finding and its importance? Animals exposed to 2% NaCl drinking solution develop hypertension, with dominance of sympathetic outflow and high [Na ] in the cerebrospinal fluid, but without changes in the blood volume. The phenotype of salt-dependent hypertension might be related to accumulation of [Na ] in the cerebrospinal fluid, which makes it an interesting animal model in which to study the neuronal pathways involved in control of the circulation in osmotic challenge conditions.
Evidence suggests that hypertension induced by high salt intake is correlated with an autonomic imbalance that favours sympathetic hyperactivity and an increase in vascular resistance, indicating a neurogenic component to this pathology. Although there are several animal models in which to study salt-induced hypertension with prolonged exposure to a high-sodium diet, here we sought to investigate whether the increase in arterial blood pressure of rats subjected to a short exposure to high salt, with 2% NaCl drinking solution instead of water, relies on changes in the circulating blood volume. Male Wistar rats were divided randomly into three groups: euhydrated (EU, n = 10), salt loaded (SL, n = 13) and water deprived (WD, n = 6). The SL rats exhibited a significant increase in mean arterial blood pressure, with a large low-frequency component of systolic arterial blood pressure variability, when compared with the EU group. Circulating blood volume did not differ between SL and EU rats, but it was lower in WD rats. Compared with EU rats, the [Na ] in cerebrospinal fluid was higher in SL rats and similar in magnitude to the WD rats. Plasma [Na ] did not differ between SL and EU rats, but it was higher in WD rats. Collectively, our data suggest that the hypertension induced by a short exposure to high salt intake closely resembles a neurogenic mechanism, but not a blood volume-dependent mechanism, with cumulative [Na ] in the cerebrospinal fluid that could be associated with changes in the neurochemistry of autonomic nuclei, which are highly susceptible to osmotic stress related to high salt consumption.
本研究的核心问题是什么？在饮水中摄入 2%的盐水使大鼠产生高血压的心血管表型是否为血容量依赖性高血压？主要发现及其重要性是什么？暴露于 2%盐水饮水中的动物会发生高血压，其特征为交感神经输出增加和脑脊液中[Na+]升高，但血容量无变化。盐依赖性高血压的表型可能与脑脊液中[Na+]的积累有关，这使其成为研究在渗透挑战条件下控制循环的神经元途径的有趣动物模型。
有证据表明，高盐摄入引起的高血压与自主神经失衡有关，这种失衡有利于交感神经活性增加和血管阻力增加，表明这种病理存在神经源性成分。尽管有几个动物模型可以研究长时间暴露于高盐饮食引起的盐诱导性高血压，但我们在此试图研究短时间暴露于高盐（用 2%盐水代替水）的大鼠动脉血压升高是否依赖于循环血量的变化。雄性 Wistar 大鼠随机分为三组：正常水合组（EU，n=10）、盐水负荷组（SL，n=13）和限水组（WD，n=6）。与 EU 组相比，SL 组大鼠的平均动脉血压显著升高，且收缩压动脉血压变异性的低频成分较大。SL 和 EU 大鼠的循环血量无差异，但 WD 大鼠的循环血量较低。与 EU 大鼠相比，SL 大鼠的脑脊液[Na+]较高，与 WD 大鼠相似。SL 和 EU 大鼠的血浆[Na+]无差异，但 WD 大鼠的血浆[Na+]较高。总之，我们的数据表明，短期高盐摄入引起的高血压与神经源性机制密切相关，而不是血容量依赖性机制，累积的脑脊液[Na+]可能与自主神经核的神经化学变化有关，而自主神经核对与高盐摄入相关的渗透应激高度敏感。
